Fear is a normal reaction to danger, but when fear response are[unreadable] routinely expressed inappropriately, a fear or anxiety disorder exists.[unreadable] One of the leading ideas is that anxiety disorders reflect malfunctions[unreadable] in the brain system that evolved to detect danger and execute defense[unreadable] responses. Many of the stimuli that activate this system, the fear[unreadable] system, in humans are not hard-wired into the brain s circuitry, but[unreadable] instead are learned about through experience. The proposed research is[unreadable] thus aimed at understanding how the brain learns and stores information[unreadable] about danger. Classical fear conditioning is used as a behavioral[unreadable] procedure through which an innocuous stimulus (a conditioned stimulus)[unreadable] when associated with an aversive event (an unconditioned stimulus),[unreadable] acquires the capacity to elicit fear reactions. The hypothesis being[unreadable] tested is that the amygdala plays an essential role in the plasticity[unreadable] that underlies fear conditioning. This hypothesis is supported by[unreadable] considerable evidence, but some fundamental questions concerning its[unreadable] validity remain unanswered. The aims of this proposal are to clarify[unreadable] issues concerning the neural pathways which an acoustic conditioned[unreadable] stimulus is transmitted to the amygdala, the patterns of information[unreadable] flow within the amygdala, the necessity of the amygdala for the[unreadable] acquisition and storage process, and the nature of neural coding in[unreadable] various components of the circuitry. Together, these studies represent[unreadable] an integrated, multidisciplinary research program aimed at understanding[unreadable] the nature of fear and will hopefully provide information that will be[unreadable] useful in preventing or treating disorders.